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首页> 外文期刊>Rheumatology Advances in Practice >All That glitters is not gold
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All That glitters is not gold

机译：所有闪光的不都是金子

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Introduction Inflammatory muscle disease is a rare but well-recognised manifestation of systemic vasculitis. It can present as focal myositis or symmetrical proximal muscle involvement seen in polymyositis and dermatomyositis. Investigative findings in inflammatory myositis include raised creatine kinase, abnormal electromyography and muscle biopsy. MR scans can identify muscle abnormality, oedema, fibrosis and the extent of muscle involvement, and are routinely requested to evaluate patients with suspected or definite myositis. They also guide us to the appropriate muscles to biopsy. MR scans are not diagnostic of myositis and treating clinicians must be aware of its mimics. Our case demonstrates one such mimic. Case description A 59-year-old male patient under care of the renal physicians for ANCA-associated vasculitis complained of bilateral thigh pain. He had completed IV cyclophosphamide therapy (CYCLOPs protocol) for vasculitis affecting lungs, kidneys, and ENT. He was taking 30mg prednisolone and 100mg azathioprine daily. He denied muscle weakness, paraesthesia, or sensory symptoms. There was no muscle wasting, fasciculation, or sensory loss. Deep tendon reflexes were normal. 8-months prior, he was investigated for right hip pain and paraesthesia with MR spine and right hip, and neurophysiological studies. Investigations confirmed lumbar disc prolapse with neurophysiology in keeping with right L4 denervation changes. He had been treated with physiotherapy and daily pregabalin, duloxetine, and co-codamol. Renal physicians requested MR thigh, which was reported as muscle oedema over the long length of the right vastus medialis and lateralis, suggesting myositis. Rheumatology referral for myositis related to vasculitis was made. He was PR3+ve-3IU/ml (improved), ESR-2, CRP-4.6mg/L, CK-94U/L. EGFR remained stable at 66ml/min. Clinical features were not supportive of myositis and systemic vasculitis was in remission. The decision was made to discuss scans at the rheumatology- radiology meeting before considering a change in immunosuppression or muscle biopsy. Radiologists felt that findings of localised muscle group involvement suggested a neurogenic cause rather than primary muscle inflammation. They had reviewed MR lumbar spine done previously which had identified degenerative changes with right foraminal stenosis at L3-4 and L4-5 disc space.?Electrophysiology showed chronic neurogenic changes of moderate severity in predominately L4 innervated muscles – vastus medialis and adductor magnus of the right lower limb. Findings were supportive of chronic right L4 radiculopathy and not a vasculitic neuropathy or myositis. Hence immunosuppression was left unchanged. He responded well to physiotherapy and did not require spinal surgical intervention. Discussion Our patient developed bilateral thigh pain in the setting of vasculitis. MR imaging was suggestive of myositis. Differential diagnoses included myositis related to vasculitis, primary focal myositis followed by vasculitic neuropathy, or denervation changes due to nerve entrapment. MRI is an excellent imaging modality for skeletal muscle due to its soft tissue resolution. It helps in narrowing differentials in skeletal muscle pathology, clinicians are able to identify individually affected muscle or muscle groups, give information about active muscle inflammation and/or damage. They can assist clinicians in targeting muscle for biopsy. Pattern and extent of muscle involvement can provide valuable clue to peripheral nerve or root lesion. Though MR suggested myositis, clinical assessment was not typical of myositis. Our patient had no systemic features of active vasculitis, which are concurrently present in 80% of vasculitic neuropathies. Neurophysiology in vasculitic neuropathy typically shows evolving multifocal axonal neuropathy with reduced compound muscle action potential amplitudes.?His electrophysiology was of chronic denervation in the L4 region and explained the patient’s clinical symptoms and MR findings. For skeletal muscle pathology, three key patterns of MRI signal intensity include mass lesions, fatty infiltration and muscular oedema. In this patient, recognising unilateral muscle oedema localised to the vastus medialis and lateralis (innervated by L4) was key to diagnosis. Other muscles innervated by L4 nerve root are iliopsoas, tibialis anterior and posterior. Neurophysiology did demonstrate changes in iliopsoas muscle. In this patient, the muscle atrophy common to lower motor neurone lesions was not present. This is possible when partial denervation or reinnervation occurs, changes noted on neurophysiological studies in this patient. Our case shows MR evidence of myositis may not always equate to inflammatory myositis. In this patient, awareness of the radiological mimics of myositis avoided a muscle biopsy or further immunosuppression. Key learning points Myositis is an uncommon but recognised manifestation of systemic vasculitis. Chronic
机译：引言炎性肌肉疾病是一种罕见但公认的系统性血管炎表现。它可以表现为局灶性肌炎或对称性近端肌肉受累，见于多肌炎和皮肌炎。炎性肌炎的调查结果包括肌酸激酶升高，肌电图异常和肌肉活检。 MR扫描可识别肌肉异常，水肿，纤维化和肌肉受累程度，并常规要求对怀疑或确定性肌炎的患者进行评估。他们还指导我们进行适当的肌肉活检。 MR扫描不能诊断为肌炎，临床医生必须意识到其模仿。我们的案例证明了这样一种模仿。病例描述一名59岁的男性患者在接受ANCA相关血管炎的肾脏内科医师的护理下，抱怨双侧大腿疼痛。他已完成IV环磷酰胺治疗（CYCLOPs方案）用于影响肺，肾和ENT的血管炎。他每天服用30毫克泼尼松龙和100毫克硫唑嘌呤。他否认肌肉无力，感觉异常或感觉症状。没有肌肉萎缩，束缚或感觉丧失。深层肌腱反射正常。此前8个月，他接受了MR脊柱和右髋的右髋疼痛和感觉异常以及神经生理学研究。调查证实腰椎间盘突出症的神经生理学与正确的L4神经支配变化保持一致。他已经接受了物理疗法和每日普瑞巴林，度洛西汀和co-codamol的治疗。肾内科医生要求MR大腿，据报道这是右大右内侧和外侧肌长段的肌肉水肿，提示为肌炎。风湿病转诊为与血管炎相关的肌炎。他是PR3 + ve-3IU / ml（改善），ESR-2，CRP-4.6mg / L，CK-94U / L。 EGFR保持稳定在66ml / min。临床特征不支持肌炎，全身血管炎已缓解。在考虑改变免疫抑制或肌肉活检之前，决定在风湿病学放射学会议上讨论扫描。放射科医生认为，局部肌肉群受累的发现提示是神经性原因而不是原发性肌肉发炎。他们回顾了以前做过的MR腰椎，发现腰椎间盘狭窄在L3-4和L4-5椎间盘间隙发生了退行性改变。电生理学显示，在L4神经支配的肌肉中，中度严重程度呈慢性神经原性改变-股内侧中枢和内收肌。右下肢。研究结果支持慢性右L4神经根病，而不支持血管性神经病或肌炎。因此免疫抑制作用保持不变。他对理疗反应良好，不需要脊柱外科手术。讨论我们的患者在血管炎的情况下出现了双侧大腿疼痛。 MR显像提示肌炎。鉴别诊断包括与血管炎有关的肌炎，原发性局灶性肌炎，然后是血管性神经病变，或由于神经束缚引起的神经支配改变。 MRI由于其软组织分辨率而成为骨骼肌的出色成像方式。它有助于缩小骨骼肌病理学的差异，临床医生能够识别出个体受影响的肌肉或肌肉群，提供有关活动性肌肉炎症和/或损伤的信息。他们可以帮助临床医生针对肌肉进行活检。肌肉受累的方式和程度可为周围神经或根部病变提供有价值的线索。尽管MR提示患有肌炎，但临床评估并非典型的肌炎。我们的患者没有活动性血管炎的全身特征，而这些特征同时存在于80％的血管性神经病中。血管性神经病变的神经生理学通常表现为不断发展的多灶性轴突性神经病变，其复合肌肉动作电位幅度降低。他的电生理学是L4区域的慢性神经支配，并解释了患者的临床症状和MR发现。对于骨骼肌病理，MRI信号强度的三个关键模式包括肿块病变，脂肪浸润和肌肉水肿。在该患者中，识别单侧肌水肿位于股内侧肌和外侧肌（受L4支配）是诊断的关键。 L4神经根支配的其他肌肉是are肌，胫骨前和后。神经生理学确实显示了肌的变化。在该患者中，不存在下运动神经元病变常见的肌肉萎缩。当发生部分神经支配或神经支配时，这是可能的。我们的病例表明，肌炎的MR证据可能并不总是等同于炎性肌炎。在该患者中，了解肌炎的放射学模拟避免了肌肉活检或进一步的免疫抑制。学习要点肌炎是系统性血管炎的罕见但公认的表现。慢性的

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